Periodontitis and rheumatoid arthritis (RA) appear to share many pathologic features. The common pathologic mechanisms of these two common chronic conditions are explored. Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and RA. While this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to experience more significant periodontal problems compared to their non-RA counterparts, and vice versa. A case is made that these two diseases could be very closely related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of such dysfunction is still unknown.
Nonetheless, there is accruing evidence to support the notion that both conditions manifest as a result of an imbalance between proinflammatory and anti-inflammatory cytokines. As a result, new treatment strategies are expected to emerge for both diseases that may target the inhibition of proinflammatory cytokines and destructive proteases. The clinical implications of the current data dictate that patients with RA should be carefully screened for their periodontal status.
Rheumatoid arthritis is also a chronic destructive inflammatory disease characterized by the accumulation and persistence of an inflammatory infiltrate in the synovial membrane that leads to synovitis and the destruction of the joint architecture resulting in impaired function. As a systemic disease, RA has extra-articular manifestations in systems such as the pulmonary, ocular, vascular, and other organs or structures that may be affected by the inflammatory process. The current paradigm for RA includes an initiating event (possibly a microbial exposure or a putative autoantigen) leading to significant synovial inflammation and tissue destruction. As for periodontitis, there is an accumulation of inflammatory cells (T and B lymphocytes, neutrophils, and monocytes), tissue edema, endothelial cell proliferation, and matrix degradation. RA is also modified by systemic, genetic, and environmental variables.
The periodontal diseases range from the relatively benign form of gingivitis to aggressive periodontitis. Many of these conditions are not only a threat to the dentition, but may also be a threat to general health. There are reports suggesting increased prevalence of diabetes, atherosclerosis, myocardial infarction, and stroke in patients with periodontal disease. Thus, the likelihood of periodontal disease being associated with systemic diseases is becoming established fact. All forms of inflammatory periodontal disease are associated with chronic inflammation (accumulation of B and T lymphocytes as well as monocytes and neutrophils), resulting in destruction of the periodontal ligament and bone. If left untreated, significant tissue damage occurs, and the affected teeth can become loose and may be lost if the disease continues to be active. What is particularly curious about this disease is the great variability in presentation. Because of its multifactorial nature, which is modified by systemic, environmental, and microbiological factors, not all individuals are affected to the same degree despite the ubiquitous presence of dental plaque.
Managing acute pathology of often relies on the addressing underlying pathology and symptoms of the disease. There is currently a need in the art for new compositions to treatment of periodontitis and rheumatoid arthritis.